In the prophage state, the nucleic acid of a temperate bacteriophage is replicated in synchrony with the DNA of the host bacterium; when the host cell divides, each daughter receives one copy of phage DNA. This is accomplished for all of the well-studied phages by physical insertion of the virus DNA into the genome of the host. Bacteriophage P1 is the only known exception. Somehow, the P1 prophage contrives to remain stably integrated with the replication machinery of the host without being stably attached to the bacterial genome. The basic purpose of this research is to gain an understanding of this different kind of host-cell interaction and of the potential influence of environmental factors on it. I believe that if the control of lysogeny by P1 can be elucidated it may serve as a prototype for a whole class of other viruses and plasmids that are stably associated with their hosts. It is not unlikely that this system of replication control will turn out to be used by some kinds of carcinogenic viruses in animal cells. To continue this project, we plan to test a model for bipartite control of prophage immunity, similar to that suggested for P22. The studies will include isolation and characterization of putative antirepressor mutants and mutants controlling antirepressor. BIBLIOGRAPHIC REFERENCES: Scott, J.R. (1975) Superinfection Immunity and Prophage Repression in Phage P1. Virology 65, 173-178. Scott, J.R., Kropf, M. M. and Mendelson, L. Virology. Clear Plaque Mutants of Phage P7. In press.